关键词: 巨噬细胞, 结核分枝杆菌, 自噬

Abstract: Objective To explore the role of macrophage autophagy induced by Mycobacterium tuberculosis (TB) infection. 
Methods Peripheral blood samples were collected from 15 active TB patients and 15 healthy volunteers respectively. The expression of LINC00943 was detected by real time quantitative reverse transcription polymerase chain reaction (qRT-PCR). Autophagy was detected by immunofluorescence and transmission electron microscopy. Expressions of LC3-Ⅰ, LC3-Ⅱ and Toll-like receptor 4 (TLR4)/ nuclear factor kappa-B (NF-κB) pathway-related proteins were detected by Western blot. Cell viability was detected by cell counting kit-8 (CCK-8), and apoptosis was detected by flow cytometry. 
Results Compared with the healthy control group, monocyte apoptosis was reduced and autophagy was enhanced in TB patients. Compared with the monocytes of healthy controls, the expression of LINC00943, TLR4 and MyD88 in the monocytes of TB patients was significantly upregulated. Overexpression of LINC00943 induced macrophage autophagy, and LINC00943 regulated macrophage autophagy by modulating the TLR4/NF-κB pathway. TLR4/NF-κB pathway inhibitor treatment could reverse the promotion of macrophage autophagy by LINC00943. 
Conclusion LINC00943 inhibits macrophage autophagy in tuberculosis by modulating the TLR4/NF-κB pathway, suggesting a new strategy for treating the occurrence of active TB caused by immune escape from Mycobacterium tuberculosis. 

Key words: mycobacterium tuberculosis, macrophages, autophagy